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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reports about anaphylactic and anaphylactoid reactions to rocuronium have increased recently. We report two new cases of documented grade III anaphylaxis, leading to death in one patient. The first case occurred in an 81-year-old ASA II woman scheduled for emergency abdominal surgery. Severe hypotension and tachycardia were observed after rocuronium, without bronchospasm. Neosynephrine allowed rapid resuscitation, and the patient recovered fully. The second patient was a 64-year-old ASA II man scheduled for abdominal surgery. Severe haemodynamic instability and bronchospasm occurred after rocuronium. Despite immediate life support, the postoperative period was complicated by persistent low systolic pressure, acute respiratory distress syndrome, acute renal failure, disseminated intravascular coagulation and pancreatitis, leading to the death of the patient.
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PMID:Anaphylaxis to rocuronium. 1256 31

Severe pancreatitis is frequently associated with acute lung injury (ALI) and the respiratory distress syndrome. The role of granulocyte-macrophage colony-stimulating factor (GM-CSF) in mediating the ALI associated with secretagogue-induced experimental pancreatitis was evaluated with GM-CSF knockout mice (GM-CSF -/-). Pancreatitis was induced by hourly (12x) intraperitoneal injection of a supramaximally stimulating dose of the cholecystokinin analog caerulein. The resulting pancreatitis was similar in GM-CSF-sufficient (GM-CSF +/+) control animals and GM-CSF -/- mice. Lung injury, quantitated by measuring lung myeloperoxidase activity (an indicator of neutrophil sequestration), alveolar-capillary permeability, and alveolar membrane thickness was less severe in GM-CSF -/- than in GM-CSF +/+ mice. In GM-CSF +/+ mice, pancreas, lung and serum GM-CSF levels increase during pancreatitis. Lung levels of macrophage inflammatory protein (MIP)-2 are also increased during pancreatitis, but, in this case, the rise is less profound in GM-CSF -/- mice than in GM-CSF +/+ controls. Administration of anti-MIP-2 antibodies was found to reduce the severity of pancreatitis-associated ALI. Our findings indicate that GM-CSF plays a critical role in coupling pancreatitis to ALI and suggest that GM-CSF may act indirectly by regulating the release of other proinflammatory factors including MIP-2.
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PMID:In vivo evidence for the role of GM-CSF as a mediator in acute pancreatitis-associated lung injury. 1216 73

Lung injury is the most pertinent manifestation of extra-abdominal organ dysfunction in pancreatitis. The propensity of this retroperitoneal inflammatory condition to engender a diffuse and life-threatening lung injury is significant. Approximately one third of patients will develop acute lung injury and acute respiratory distress syndrome, which account for 60% of all deaths within the first week. The variability in the clinical course of pancreatitis renders it a vexing entity and makes demonstration of the efficacy of any specific intervention difficult. The distinct pathologic entity of pancreatitis-associated lung injury is reviewed with a focus on etiology and potential therapeutic maneuvers.
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PMID:Lung injury in acute pancreatitis: mechanisms, prevention, and therapy. 1238 18

Arsenic poisoning was diagnosed in a 26-year-old man who had been criminally intoxicated over the last two weeks preceding admission by the surreptitious oral administration of probably 10 g of arsenic trioxide (As2O3). The patient developed severe manifestations of toxic hepatitis and pancreatitis, and thereafter neurological disorders, respiratory distress, acute renal failure, and cardiovascular disturbances. In addition to supportive therapy, extrarenal elimination techniques and chelating agents were used. Dimercaprol (BAL) and dimercaptosuccinic acid (DMSA or succimer) were used simultaneously as arsenic chelating agents for two days, and thereafter DMSA was used alone. DMSA was administered by intravenous (20 mg/kg/d for five days, then 10 mg/kg/d for six days) and intraperitoneal route. Intravenous DMSA infusion was well tolerated and resulted in an increase in arsenic blood concentration immediately after the infusion. Continuous venovenous hemofiltration combined with hemodialysis, and peritoneal dialysis were proposed to enhance arsenic elimination. It was calculated that over an 11-day period 14.5 mg arsenic were eliminated by the urine, 26.7 mg by hemodialysis, 17.8 mg by peritoneal dialysis, and 7.8 mg by continuous venovenous hemofiltration. These amounts appeared negligible with regard to the probable ingested dose. The patient died on day 26 from the consequences of multiple organ failure, with subarachnoid hemorrhage and generalized infection caused by Aspergillus fumigatus.
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PMID:Acute arsenic poisoning treated by intravenous dimercaptosuccinic acid (DMSA) and combined extrarenal epuration techniques. 1264 60

Acute thrombotic thrombocytopenic purpura (TTP) is a life-threatening disorder that has previously been described associated with various types of surgery. An association between total abdominal hysterectomy (TAH) and TTP has never been reported. Thrombotic thrombocytopenic purpura is classically characterized by thrombocytopenia, microangiopathic hemolytic anemia, fever, azotemia and neurological manifestations. Atypical manifestations of TTP include hepatitis, pancreatitis, acute respiratory distress syndrome, non-occlusive mesenteric ischemia and peripheral digital ischemia. This case report describes the occurrence of acute TTP following TAH and bilateral salpingo-oopherectomy, which manifested with typical and atypical features (i.e. hepatitis, pancreatitis). Plasma exchange therapy resulted in the complete resolution of the process.
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PMID:A case report of total abdominal hysterectomy resulting in acute thrombotic thrombocytopenic purpura with pancreatitis and hepatitis: complete resolution with plasma exchange therapy. 1292 16

Pulmonary thromboembolism (PTE) is rarely diagnosed in cats, and the clinical features of the disease are not well known. PTE was diagnosed at postmortem examination in 17 cats, a prevalence of 0.06% over a 24-year period. The age of affected cats ranged from 10 months to 18 years, although young (<4 years) and old (>10 years) cats were more commonly affected than were middle-aged cats. Males and females were equally affected. The majority of cats with PTE (n = 16) had concurrent disease, which was often severe. The most common diseases identified in association with PTE were neoplasia, anemia of unidentified cause, and pancreatitis. Cats with glomerulonephritis, encephalitis, pneumonia, heart disease, and hepatic lipidosis were also represented in this study. Most cats with PTE demonstrated dyspnea and respiratory distress before death or euthanasia, but PTE was not recognized ante mortem in any cat studied. In conclusion, PTE can affect cats of any age and is associated with a variety of systemic and inflammatory disorders. It is recommended that the same clinical criteria used to increase the suspicion of PTE in dogs should also be applied to cats.
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PMID:Pulmonary thromboembolism in cats. 1532 May 93

A characteristic feature of all inflammatory disorders is the excessive recruitment of leukocytes to the site of inflammation. The loss of control in trafficking these cells contributes to inflammatory diseases. Leukocyte recruitment is a well-orchestrated process that includes several protein families including the large cytokine subfamily of chemotactic cytokines, the chemokines. Chemokines and their receptors are involved in the pathogenesis of several diseases. Acute lung injury that clinically manifests as acute respiratory distress syndrome (ARDS) is caused by an uncontrolled systemic inflammatory response resulting from clinical events including major surgery, trauma, multiple transfusions, severe burns, pancreatitis, and sepsis. Systemic inflammatory response syndrome involves activation of alveolar macrophages and sequestered neutrophils in the lung. The clinical hallmarks of ARDS are severe hypoxemia, diffuse bilateral pulmonary infiltrates, and normal intracardiac filling pressures. The magnitude and duration of the inflammatory process may ultimately determine the outcome in patients with ARDS. Recent evidence shows that activated leukocytes and chemokines play a key role in the pathogenesis of ARDS. The expanding number of antagonists of chemokine receptors for inflammatory disorders may hold promise for new medicines to combat ARDS.
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PMID:Chemokines in acute respiratory distress syndrome. 1559 Oct 40

A 53-year-old woman was admitted with respiratory distress. For several years, she had chronic alcoholic pancreatitis with ductal stones that were treated with a stent and with shockwave lithotripsy. Both treatments were unsuccessful, and the pancreatitis was complicated with an infected pseudocyst. The pancreatic head had to be resected, which was complicated with recurrent subphrenic abscesses. She then was admitted with respiratory distress and initially diagnosed with pneumonia of the right lower lobe. Further investigations showed supradiaphragmatic and subdiaphragmatic air-fluid levels. In both collections Streptococcus milleri was cultured, and subsequently the patient was diagnosed with a fistula connecting the subdiaphragmatic abscess with pulmonary tissue. This was treated with intravenous amoxicillin/clavulanate and drainage of the subdiaphragmatic collection. She did not develop a pulmonary empyema, because multiple adhesions, which were due to recurrent abscesses after pancreatic surgery, prevented breakthrough into the pleural cavity.
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PMID:Transphrenic fistulization of a subphrenic abscess to lung parenchyma. 1586 69

The acute respiratory distress syndrome (ARDS) is a life-threatening syndrome that may occur in any patient without any predisposition and that is mostly triggered by underlying processes such as sepsis, pneumonia, trauma, multiple transfusions, and pancreatitis. ARDS is defined by (1) acute onset, (2) bilateral infiltrates in chest x-rays, (3) absence of left ventricular failure, and (4) severe arterial hypoxemia with a PaO2/FiO2 ratio less than 200 mmHg. Still, ARDS is feared (mortality 30-40%) and relatively frequent (incidence between 13.5 per 100,000 to 75 per 100,000). Acute lung injury (ALI) describes a similar, but less severe, clinical condition, with PaO2/FiO2 values between 200 and 300 mmHg. Despite ongoing and intensive scientific research in this area, the mechanisms underlying ALI/ARDS are still not completely understood, and until recently, there were no studies demonstrating any beneficial effect of a single treatment modality in ARDS. The recent report that a specific approach to ventilatory support can significantly reduce mortality in ARDS underscores the need for better understanding of the pathophysiological events occurring in this syndrome. This review therefore summarizes the current pathophysiological concepts underlying the evolution of acute hypoxemic respiratory failure and focuses on: (1) possible reasons for the development of ALI/ARDS; (2) cellular and humoral mediator responses leading to a sustained and self-perpetuating inflammation of the lung; (3) consequences with regard to fluid balance, pulmonary perfusion, ventilation, and efficiency of gas exchange; and (4) mechanisms underlying the aggravating complications commonly seen in ARDS, especially ventilator-associated lung injury, ventilator-associated pneumonia, and lung fibrosis.
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PMID:Pathophysiology of acute lung injury. 1608 77

We report 13 severely disabled children with acute respiratory distress syndrome, who were treated at the Department of Pediatrics, Niigata City General Hospital between 1995 and 2002. The children ranged in age from 1 year to 16 years. All were non-ambulant. Chronic aspiration and gastro-esophageal reflux were recognized in 12 patients. Patients had the rapid onset of dyspnea refractory to oxygen therapy. Diffuse bilateral lung infiltrates were present on chest X-ray. Predisposing events included sepsis (3 patients), pneumomia (7 patients), pancreatitis (1 patient) and two children with other infections. All required mechanical ventilation for periods of 3-26 days and received oxygen for 5-64 days. Steroid therapy and surfactant therapy were given to eight and three patients, respectively. Only one patient developed an air leak complication. Despite intensive care, three children died, one underwent tracheostomy and nine recovered completely. Acute respiratory distress syndrome is a commonly recognized cause of acute respiratory failure following a variety of insults. It is characterized by the acute onset of dyspnea refractory to oxygen therapy, and diffuse lung infiltrates. Children with severe motor and intellectual disabilities had various complications. In this study, chronic aspiration and gastro-esophageal reflux are considered to be one of predisposing factors triggering acute respiratory distress syndrome in children with severe motor and intellectual disabilities. Although acute respiratory distress syndrome was considered to be a not infrequent occurrence, its mortality rate might be low despite the severity of the disease in children with severe motor and intellectual disabilities. Acute respiratory distress syndrome can be a complication seen in severely disabled children.
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PMID:Acute respiratory distress syndrome in children with severe motor and intellectual disabilities. 1647 54


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